The eating disorders anorexia nervosa and bulimia nervosa have some of the highest mortality rates (i.e., > 10 percent) of any psychiatric illness. The overall purpose of the proposed study is to increase understanding of the epidemiology of these disorders by examining genetic and environmental risk factors using a developmental, behavioral genetic approach. Data for this project come from 680 11 year-old twins participating in the population-based, longitudinal Minnesota Twin Family Study. Twins from this larger project were assessed at three-year intervals following baseline (i.e., ages 11, 14, 17), and data from all three timepoints will be used in analyses. The first aim of the proposed study is to examine developmental differences in genetic and environmental influences on disordered eating attitudes and behaviors across adolescence (i.e. at ages 11, 14, and 17). It is hypothesized that genetic influences will increase and environmental influences will decrease in magnitude across these three adolescent ages. The second aim is to determine the role of puberty in these developmental differences. It is hypothesized that eating pathology will show negligible genetic influence in pre-pubertal twins, but significant genetic effects in post-pubertal twins. Structural equation modeling will be used to examine each of these first two hypotheses. The final aim of the proposed project is to identify specific genetic and environmental risk factors for eating disorders by examining Time 1 (age 11) psychiatric (depression, anxiety, and disordered eating), temperamental (negative emotionality, positive emotionality, and constraint), physical/maturational (body mass index (BMI), pubertal status), and family (relationships with parents, marital discord) predictors of Time 3 (age 17) eating disorder status. The nature (i.e., genetic versus environmental) of significant risk factors will then be examined. It is hypothesized that anxiety disorders, negative emotionality, pubertal status, and BMI will be the most significant predictors of eating pathology. Further, risk factor/eating disorder covariations are hypothesized to be due to common genetic rather than common environmental factors. These last hypotheses will be tested using logistic regression analyses as well as structural equation modeling. Findings from this study will significantly increase understanding of developmental risk factors for eating disorders and potentially inform intervention and prevention efforts aimed at their amelioration.